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71 Cards in this Set

  • Front
  • Back
anaplasia
an exaggerated form of dysplasia that can be observed in malignant cells that includes varying degrees of cytologic and nuclear atypia, alteration in the shape and size of the cell and/or nucleus, loss of cell orientation, and abnormal mitoses
anthracosis
accumulation in the lungs from inhaled smoke or coal dust; miner’s lung
apoptosis
a distinctive form of cell death that involves individual cells or small clusters of; active, energy-dependent process under strict regulatory control that does not illicit an inflammatory response
apoptotic body
small, membrane-bound segment of a cell that results from apoptosis; phagocytized by macrophages via receptor binding
autolysis
cellular destruction caused by endogenous enzymes
autophagic vacuole
formed by fusion of a lysosome with a cytoplasmic structure to digest intracellular material
autophagy
digestion of cellular material by enzymes of the same cell
caspaces
a family of intracellular proteolytic enzymes that mediate the apoptotic process present within the cytosol in their inactive form (procaspaces)
catabolism
destructive metabolism in which complex materials are broken down to release energy
chromatin
the finely-dispersed state in which DNA can be found in the nucleus of a resting (non-dividing) cell
crepitation
– to make a crackling sound due to air bubbles beneath the surface of the skin
cytokine
regulatory protein released by cells of the immune system that act as intercellular mediators of the immune response
cytoskeleton
an integral part of the cytoplasm that allows for cell motility and maintains cell structure, consisting of microfilaments, cell-type specific intermediate filaments, and microtubules
cytosol
the amorphous ground substance of the cytoplasm consisting of water, nutrients, carbohydrates, lipids, and proteins; also the location of cellular organelles
etiology
cause or origin of a disease
ferritin
ferric iron-apoferritin protein complex involved in normal iron absorption and storage
frostbite
damaged vascular endothelium increases vascular permeability, leading to edema and blister formation
heterolysis
cellular destruction caused by exogenous enzymes
homeostasis
ability to maintain internal equilibrium by adjusting physiological processes
heterophagy
digestion within a cell of a substance taken into the cell by phagocytosis from the outside environment
karyolysis
chromatin dissolution, definitive morphologic evidence of irreversible cell injury and death
karyorrhexis
chromatin fragmentation, definitive morphologic evidence of irreversible cell injury and death
parenchyma
generally composed of epithelial cells, this tissue is the distinctive (often functional) cells of an organ
pathogenesis
the development of a diseased condition
psammoma body
small, concentrically laminated sphere of calcium, representing a calcium deposit
pyknosis
dense chromatin condensation, definitive morphologic evidence of irreversible cell injury and death
residual body
remnant of material that lysosomes are unable to digest found in the cytoplasm
stroma
generally composed of mesenchymal connective tissue cells, this tissue provides the structural framework of an organ
hydropic change
an exaggerated form of cellular swelling in which ER looks like water vacuoles; surrounding microvasculature may be compressed and add to cellular injury
steatosis
is an absolute increase in lipids within parenchymal cells, usually in the liver but sometimes in the heart or kidney; different from fatty ingrowth
what is lipofuscin associated with?
brown atrophy of heart and liver
what is the clinical significance of hemosiderin?
abnormal breakdown of RBCs
compare and contrast hemochromatosis and hemosiderosis
hemosiderosis - hemosiderin is present in excessive amounts, result of chronic hemolysis of RBCs, found in heart, liver, pancreas, skin
hemochromatosis - severe metabolic disorder, defect in normal iron metabolism, masssive iron depositions in heart, liver, pancreas, and skin that leads to cirrhosis, diabetes mellitus, bronze skin discoloration, and heart failure
what causes coagulative necrosis
inadequate cell oxygenation, often due to ischemia
what causes dry gangrene
ischemic coagulative necrosis of skin and subcutaneous tissues of extremities
what causes wet gangrene
tissue hypoxia secondary to ischemia
what causes liquefactive necrosis
bacterial infections attract neutrophils, resulting in abscesses; ischemic destruction of brain tissue
what causes caseous necrosis
infectious diseases with mycobacteria and fungi
what causes enzymatic fat necrosis
pancreatic enzymes (lipases) act on fat cells to convert triglycerides to free FAs that complex with calcium to form calcium soaps
what causes traumatic fat necrosis
traumatic rupture of fat cells followed by phagocytosis of lipid material
what causes fibrinoid necrosis
deposition of immunoglobulins, fibrinogen, and complement in blood vessel walls
what are some pro-apoptotic factors
include TNFα, glucocorticoids, chemotherapeutic drugs, free radicals, and UV radiation
what are some anti-apoptotic factors
growth factors, sex steroids, and the EB virus.
what are the factors in the extrinsic activation of caspase activity (apoptosis)
FAS protein, TNF (on cell surface), initiator procaspace - procaspace 8
what are the factors in the intrinsic activation of caspace activity (apoptosis)
mitochondrial membranes, Bcl-2 proteins, Bcl-x (both decrease) Bax and Bak both increase, cytochrome C is released, binds to Apaf-1, activates initiator procaspace 9
what is a full thickness burn?
destroy the epidermis as well as the underlying dermis and dermal appendages, so reepithelialization cannot occur. Healing takes a long time, must occur from the outside edges, and there is an increased risk of infection
what is a partial thickness burn
destroy the epidermis, but leave the basal epithelium or at least some of the dermal appendages intact, so epithelial cells can be regenerated
abrasion
friction; crushing
avulsion
tearing away of body parts
contusion
distruption of blood vessls produced by blunt force, bruising
laceration
tearing of tissue resulting from excessive stretching, leaves nerves and small vessels intact
incision
cut produced by small instrument
puncture
piercing or penetration of tissue caused by sharp instrument
dystrophic calcifications
occur in degenerating or necrotic tissue of patients with normal serum calcium levels. Calcium accumulates in irreparably damaged mitochondria; extracellular calcium deposits also develop by using membrane-bound vesicles for propagation
metastatic calcification
the deposition of calcium in normal tissues of patients with high serum calcium levels; this tends to occur in tissues with relatively alkaline pH, such as the cornea, lungs, stomach, and blood vessels.
anasarca
diffuse, generalized edema throughout the body
ascites
accumulation of fluid within the peritoneal cavity due to increased hydrostatic pressure within the portal venous system
brown induration
gross appearance of the lungs due to fibrous thickening of alveolar walls
cyanosis
bluish discoloration of tissue
diapedesis
the movement of blood cells through intact capillary walls into surrounding tissue
dyspnea
difficulty breathing, often associated with lung or heart disease
edema
accumulation of excess fluid in cells or tissues; generally starts in loose connective tissue, so one of the first signs of edema is puffiness around the eye
effusion
seeping of fluid into a body cavity or tissue
nutmeg liver
fatty change of peripheral periportal hepatocytes resulting in a mottled red-brown and yellow-tan gross appearance of the liver
orthopnea
discomfort in breathing when laying down; this is measured by the number of pillows required for a patient to breathe and sleep at night
rales/crackles
abnormal respiratory sounds associated with pulmonary edema
what happens when there is an increase in total body Na+
increased osmotic pressure of interstitial fluid → generalized edema
what happens when there is decreased serum albumin
decreased oncotic pressure of plasma protein → generalized edema
what happens when there is interference with or obstruction to venous blood flow
→ increased hydrostatic pressure of intravascular fluid → localized edema
transudate
is a protein-poor (<3 gm/dL) pale, clear yellow fluid that develops from imbalances in the normal hemodynamic forces. It’s often seen with CHF, liver disease, renal disease, and GI disorders
exudate
s a protein-rich (>3gm/dL) cloudy yellow fluid that develops from endothelial damage and alteration of vascular permeability. It’s often seen with inflammatory or immunologic disorders.